Hindawi Publishing Corporation

Neurology Research International

Volume 2013, Article ID 639280, 5 pages
http://dx.doi.org/10.1155/2013/639280

Review Article
Autonomic Nervous System in the Control of Energy Balance
and Body Weight: Personal Contributions

G. Messina,1 V. De Luca,1 An. Viggiano,2 A. Ascione,3 T. Iannaccone,1

S. Chieffi,1 and M. Monda1
1
Department of Experimental Medicine, Section of Human Physiology and Clinical Dietetic Service,
Second University of Naples, Via Costantinopoli 16, 80138 Naples, Italy
2
Faculty of Medicine, University of Salerno, Salerno, Italy
3
Faculty of Motor Sciences, University of Naples “Parthenope,” Naples, Italy

Correspondence should be addressed to M. Monda; marcellino.monda@unina2.it

Received 22 January 2013; Revised 12 March 2013; Accepted 24 March 2013

Academic Editor: Mamede de Carvalho

Copyright © 2013 G. Messina et al. This is an open access article distributed under the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

The prevalence of obesity is increasing in the industrialized world, so that the World Health Organization considers obesity as
a “pandemia” in rich populations. The autonomic nervous system plays a crucial role in the control of energy balance and body
weight. This review summarizes our own data and perspectives, emphasizing the influence exerted by autonomic nervous system on
energy expenditure and food intake, which are able to determine the body weight. Activation of the sympathetic discharge causes
an increase in energy expenditure and a decrease in food intake, while reduction of food intake and body weight loss determines
a reduction of the sympathetic activity. On the other hand, pathophysiological mechanisms of the obesity involve alterations of
the sympathetic nervous system in accordance with the “Mona Lisa Hypothesis,” an acronym for “most obesities known are low in
sympathetic activity.” Furthermore, the parasympathetic influences on the energy expenditure are analyzed in this review, showing
that an increase in parasympathetic activity can induce a paradoxical enhancement of energy consumption.

1. Introduction nervous system is involved in the control of eating behavior

Body weight stability and the associated regulatory processes
depend upon nutrient intake, but are also influenced by com-
pensatory genetic-dependent metabolic and neuroendocrine
mechanisms [1–4].
The control of the maintenance of body composition
has been the subject of a number of theories or pathways.
Systems that control food intake and/or energy expenditure
are able to influence body weight. Several substances are
able to influence food intake. The “glucostatic hypothesis”
emphasizes the role of blood glucose, considering that an
increase in glucose blood level induces a reduction of food
intake [5]. Leptin, a peptide secreted by white adipose tissue,
acts on the hypothalamic areas inducing a reduction of food
ingestion. This is in accord with the “lipostatic hypothesis”
of food intake [6, 7]. Gastrointestinal hormones also lower
food intake; this influence is known as the “hypothesis of
gastrointestinal control of food intake” [8, 9]. The autonomic
through influences exerted on the production and loss of
heat [10, 11]. Thus, the control of body temperature is strictly
associated with the control of body weight; this is in accord
with the “thermoregulatory hypothesis” of food intake [12].
On the other hand, the metabolic balance is controlled
by the autonomic nervous system, so that the vegetative
influences affect the storage and the consumption of energy.
Adipose tissue acts as an endocrine organ by producing
various signalling cytokines called adipokines (including
leptin, free fatty acids, tumour necrosis factor-𝛼, interleukin-
6, C-reactive protein, angiotensinogen, and adiponectin).
A chronic dysregulation of certain adipokines can have
deleterious effects on insulin signalling. Chronic sympathetic
overactivity is also known to be present in central obesity,
and recent findings demonstrate the consequence of an
elevated sympathetic outflow to organs such as the heart,
kidneys, and blood vessels. Chronic sympathetic nervous
system overactivity can also contribute to a further decline
2 Neurology Research International
of insulin sensitivity, creating a vicious cycle that may
contribute to the development of the metabolic syndrome
and hypertension. The cause of this overactivity is not clear,
but may be driven by certain adipokines [13]. Furthermore,
the postprandial activation of the peripheral sympathetic
nervous system is crucial to maintain energy balance. A
contribution of postprandial sympathetic activation to the
thermic effect of food is not always evident and depends on
the size and composition of the meal, with carbohydrates
having the clearest effect. Signals related to food intake from
various origins (e.g., gut, hepatoportal area, baroreceptors)
are integrated in the brain and result in increased peripheral
sympathetic outflow. It is of interest to emphasize the role of
diet composition (according to the life style of subjects) in the
level of sympathetic activation during the day in view of the
potential role of adrenergic overactivity in the pathogenesis
of obesity and its metabolic syndrome [14].
Although it is reported that low-frequency band (LF-
HRV) represents a noninvasive marker of sympathetic activ-
ity, there are recent studies which report that this assumption
is controversial. LF power may correlate more with baroreflex
function and/or stress that with the cardiac sympathetic
innervations [15, 16]. This vision should modify the interpre-
tations about the sympathetic function in the pathophysiol-
ogy of the obesity.
Since the incidence of body weight superior to normal
values is increasing in the industrialized world, the World
Health Organization considers obesity as a “pandemia” in
rich populations. Investigation into the mechanisms that con-
trol body weight give growing relevance to the possibilities
of new strategies to reduce the incidences of overweight and
obesity, which are frequently associated with metabolic and
cardiovascular diseases.
This review reports our evidences showing that the auto-
nomic nervous system controls body weight by influencing
food intake and energy consumption. The general research
project was to test influence of the autonomic nervous system
on energy balance under various conditions, which change
the sympathetic and/or parasympathetic activities.
2. Experimental Evidences
2.1. Animal Studies. The effect of intraperitoneal injection of
lysine acetylsalicylate was tested on (1) food intake and (2)
the sympathetic enhancement induced by lesion of the lateral
hypothalamus. Lysine acetylsalicylate modifies the aphagia by
increasing food intake, and it reduces the enhancements of
the sympathetic discharge induced by the lateral hypothala-
mic lesion [17]. The electrolytic lesion in the lateral hypotha-
lamus regulates body weight at a lower level. The lesioned rats
lose body weight at a faster rate than sham-lesioned controls
subjected to the same degree of food deprivation [18]. This
experiment confirms that an increase in the sympathetic
activity reduces food intake (see Scheme 1), in accord with
the findings of Bray [19]. On the other hand, these data show
that an inhibitor of prostaglandin synthesis can modify the
aphagia induced by the lesion of the lateral hypothalamus,
throughout a reduction of the sympathetic discharge.
Lesion of lateral hypothalamus
Alteration of various pathways,
including orexinergic system
Ascending Descending
projections projections
Behavioral Increase in
changes sympathetic activity
Reduction of food intake
Scheme 1: Changes in eating behavior induced by lesion of the
lateral hypothalamus.
The firing rate of sympathetic nerves to interscapular
brown adipose tissue (IBAT) was monitored both before and
after 5 g of food intake in 24 h fasted rats with a lesion of
the ventromedial hypothalamus and in 24 h fasted rats with
sham-lesion. The firing rate of nerves to IBAT increased
after food intake in sham-lesioned rats. This increase was
significantly reduced in the lesioned rats. These findings indi-
cate that the sympathetic nervous system is involved in the
postingestional activation of the sympathetic discharge, and
reduction of this activation occurs when the ventromedial
hypothalamus is lesioned [20]. A long-term reduction of
postingestional thermogenesis may contribute to the obesity
induced by this hypothalamic lesion through a decrease in
energy expenditure induced by reduced sympathetic activity
(see Scheme 2). Since there is a close relationship between
the sympathetic activity and food intake [19], a reduction
in the sympathetic response after food intake could induce
an increase of total amount of ingested food. This reduction
may be another factor in the induction of obesity due
to ventromedial hypothalamic lesions. In other words, the
increased body weight may be caused by a reduction of satiety
signals and a decrease in postingestional energy expenditure.
The firing rate of the sympathetic nerves to interscapular
brown adipose tissue and food intake were monitored in
24 h fasting male Sprague-Dawley rats before and after food
presentation. Pyrogen (500 ng of prostaglandin E1 ) or saline
was injected into the lateral cerebral ventricle immediately
before food presentation. The increase in the sympathetic
discharge due to prostaglandin E1 is associated with a
decrease in food intake [21]. The simultaneous measurement
of the sympathetic firing rate and food intake is the nicest
demonstration of the feedback between the sympathetic
nervous system and food intake. The sympathetic activity
rises before food intake terminates. This implies that the rise
in sympathetic discharge serves as an endogenous satiety
signal (see Scheme 3).
2.2. Human Studies. Vegetative modulation, expressed as
heart rate variability (HRV) power spectral analysis, was
Neurology Research International
Lesion of ventromedial hypothalamus
Reduction of Hormonal changes, Overeating
sympathetic including
activity hyperinsulinemia
Reduction of
energy expenditure
Obesity
Scheme 2: Changes in energy expenditure induced by lesion of the
ventromedial hypothalamus.
Cerebral administration of pyrogen
Effect on preoptic area and
anterior hypothalamus
Reset of thermal set-point
Increase in sympathetic activity
Reduction of food intake
Scheme 3: Changes in eating behavior induced by pyrogen injection.
analyzed in lean and obese women at premenopausal or post-
menopausal age. The HRV-power spectrum was evaluated
on a 5-min long ECG recording. The absolute values of the
spectrum were summed in the following frequencies: a low
frequency (0.04–0.15 Hz; LF) and high frequency (0.15–0.40;
HF) range. LF and HF were values used to estimate the
sympathetic and parasympathetic activity. LF and HF values
of premenopausal obese women were lower than values of
lean women. In postmenopause, LF and HF have a similar
decrease in lean and obese women, as a consequence no
difference can be found. These findings indicate a reduction
of the vegetative modulation in obese young women and the
reduction of the autonomic control regards both the sympa-
thetic and parasympathetic components [22]. The reduction
of the sympathetic branch could be an important factor
in the maintenance of obesity in premenopausal age (see
Scheme 4). Indeed, a reduction in the sympathetic activity
could be related to a low energy expenditure, so that a
reduced energetic cost could explain the higher body weight
in premenopausal women. This vision is in accordance with
the “Mona Lisa Hypothesis,” an acronym for “most obesities
known are low in sympathetic activity” [23]. In this exper-
iment, the autonomic activity of postmenopausal women is
lower than that of premenopausal subjects. This indicates that
the modifications of the autonomic modulation cannot be
3
Premenopausal age
Reduction Hormonal
of autonomic changes
activity
Increase in body weight
Scheme 4: Body weight gain during premenopausal age.
included among factors related to obesity in postmenopausal
subjects. Many experimental evidence have demonstrated
that an increase in sympathetic and thermogenic activity
reduces food intake. Therefore, the obesity can be due to
an increase in food intake associated to a reduced activity
of the sympathetic nervous system. On the other hand,
some study revealed lower respiratory sinus arrhythmia, as
evaluated by the HF-HRV spectral analysis combined with
deep breathing tests, which points to the presence of cardiac
vagal dysfunction in obese adolescents [24]. Importantly,
autonomic imbalance with decreased parasympathetic activ-
ity maybe the final common pathway in numerous conditions
associated with increased morbidity and mortality [25]. The
evaluation of cardiorespiratory interactions, in particular the
heart rate variability, can provide diagnostic information
about early subclinical autonomic dysfunction in obesity.
Sports are known to induce several adaptive modifica-
tions, including changes in the activity of the autonomic
nervous system and in resting energy expenditure (REE)
[26, 27]. The parasympathetic tone is enhanced by physical
training, so that a reduction in the heart rate (induced
by vagal influence) is considered as an index of training
status in athletes [28]. Since there are few studies concerning
the comparison between vegetative and energetic changes
of sedentary individuals and those of sportive subjects,
the influence exerted by sedentary and basketball exercise
training on the relationship between the activity of the
autonomic nervous system and REE was evaluated. REE,
body composition, and the level of activity of the autonomic
nervous system were measured before and after a period of six
months. The physical activity induced an increase in REE and
free fat mass without variations in body weight. Basketball
players showed a significant increase in the parasympathetic
activity, measured by the power spectral analysis (PSA) of the
heart rate variability (HRV). These findings (see Scheme 5)
demonstrate that REE is higher in the athletes than in
sedentary women, despite the augmented parasympathetic
activity that is usually related to lower energy expenditure
[29]. This is the first study to examine the effect of long-
term training on relationship among cardiac HRV, REE, and
body composition. In this study, an increase of the HF of the
HRV-PSA has been noted in sportive women, confirming that
exercise induces an increase of the parasympathetic activity
at resting. On the contrary, the LF of the PSA of HRV
4 Neurology Research International
Sportive activity
Increase in Hormonal
parasympathetic
activity changes
Increase in energy expenditure
Scheme 5: Changes in energy expenditure induced by sport.
has not been modified by sport activity, indicating that the
basketball does not modify the sympathetic discharge. The
increase in the parasympathetic activity is associated with
an increase in REE. This association is an important result
considering that the parasympathetic activity has generally
been demonstrated to have an inverse relation to REE [30, 31].
3. Discussion and Conclusion
The above-reported evidences indicate that the autonomic
nervous system can be considered a fundamental factor in the
regulation of food intake and body weight. The sympathetic
influence on this regulation is exerted by an influence on
body temperature; this is in accord with the “thermoregu-
latory hypothesis” of food intake. The consequences of this
hypothesis are that subjects with a high set-point of body
temperature and/or low sympathetic activity are induced
to eat a high quantity of food to elevate the sympathetic
discharge and body temperature. Conversely, subjects with a
low thermal set-point and/or a high sympathetic tone need to
introduce a lower quantity of food to reach a prefixed thermal
set-point. On the other hand, alterations of postprandial
thermogenesis due to a reduced response of sympathetic
activation can play an important role in inducing obesity. In
other words, subjects with a low postprandial sympathetic
activation need to introduce a higher quantity of foot to
reach a prefixed body temperature. Our findings support
the “Mona Lisa hypothesis” [23], which suggests that most
types of obesity are due to an alteration of the sympathetic
activity. On the other hand, being overweight increases the
sympathetic discharge that contributes to induce pathologies
related to abnormal body weight [32–34]. Furthermore, an
increase in parasympathetic activity is able to enhance energy
expenditure in sportive subjects. This indicates that not
only the sympathetic activation but also the parasympathetic
activation is able to increase energy expenditure, that in turn
influences body weight. Further studies should be addressed
to reveal new aspects of the control exerted by the autonomic
nervous system on body weight, so that innovative strategies
could be used for the prevention and therapy of obesity.
On the other hand, other factors other than the “Mona
Lisa hypothesis” must be considered in the genesis of obesity.
The “lipostatic hypothesis” indicates that adipokines such
as leptin could play a crucial role in the gain of body
weight. A reduction in leptin level signals to the brain to
increase feeding and decrease energy expenditure. Leptin is
an important factor linking energy stores to eating behavior
[35]. The “hypothesis of gastrointestinal hormones” suggests
that gut hormones are implicated in the control of body
weight. These hormones regulate appetite, energy expendi-
ture, and glucose homeostasis. They can act either via the
circulation at target peripheral tissues, by activation of the
vagus nerve, or by acting on key brain regions implicated in
energy homeostasis such as the hypothalamus and brainstem
[36, 37]. In conclusion, all factors of reported hypotheses can
cooperate synergically to induce body weight alteration [38].
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